Tardive dyskinesia.

Abstract

The basic pathogenesis of tardive dyskinesia appears to relate to chronic pharmacologic denervation of specific dopaminergic receptor sites in the striatum. The pathophysiology of the disorder relates to the resultant denervation hypersensitivity. The mainstay of treatment includes withdrawal of neuroleptics where feasible and the use of dopamine-depleting agents. Enhancement of the striatal cholinergic input offers potential ancillary benefit to the alleviation of abnormal movements. The benefit of manipulating other neurotransmitters remains experimental. Treatment of tardive dyskinesia with neuroleptics themselves is clearly treatment with the presumed offending agent, and should be avoided. This shortsighted therapy may temporarily abate the pathophysiology of the condition but serves to aggravate its pathogenesis.